Evidence map›Paper›PMID 19794969›Full record

ArticleNeoplasia (New York, N.Y.)2009

Systemic sclerosis-endothelial cell antiangiogenic pentraxin 3 and matrix metalloprotease 12 control human breast cancer tumor vascularization and development in mice.

Francesca Margheri, Simona Serratì, Andrea Lapucci, Chillà Anastasia, Betti Giusti, Marco Pucci, Eugenio Torre, Francesca Bianchini, Lido Calorini, Adriana Albini and 3 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
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  9. Article
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  15. Article
  16. Pentraxin-3 as a prognostic marker in patients with small-cell lung cancer.Medical oncology (Northwood, London, England) · 2014
    Article
  17. Article
  18. Article
  19. Humoral innate immune response and disease.Clinical immunology (Orlando, Fla.) · 2012
    Review
  20. The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Francesca MargheriDepartment of Experimental Pathology and Oncology, University of Florence, 50134 Florence, Italy.
Simona Serratì
Andrea Lapucci
Chillà Anastasia
Betti Giusti
Marco Pucci
Eugenio Torre
Francesca Bianchini
Lido Calorini
Adriana Albini
Agostina Ventura
Gabriella Fibbi
Mario Del Rosso
University of Florence · ITMultiMedica · ITTecnologie Avanzate (Italy) · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that endothelial cell matrix metalloprotease 12 (MMP12) and pentraxin 3 (PTX3) overproduction is the main alteration accounting for reduced proneness to angiogenesis in systemic sclerosis (SSc). On this basis, we stably transfected MMP12 and PTX3 in two breast cancer cell lines expressing very low amounts of the target molecules when compared with normal breast epithelial cells, relying on the hypothesis that antiangiogenic molecules released by cancer cells could confer an SSc-like antiangiogenic pattern on target endothelial cells. In Matrigel Boyden chamber invasion and capillary morphogenesis studies, transfected clones reduced endothelial cell invasion and capillary tube formation, which were abolished by tumor cell populations expressing both molecules. The Matrigel sponge assay, performed in vivo in C57/BL6 mice by injecting aliquots of lyophilized culture medium of transfected clones, indicated a similar reduction in angiogenesis. Functional studies have shown that endothelial cells treated with a culture medium of MMP12-expressing clones underwent cleavage of urokinase-type plasminogen activator receptor domain 1 which is indispensable to angiogenesis. We did not observe angiostatin production from plasminogen under the same experimental conditions. PTX3-overexpressing clones showed a powerful anti-fibroblast growth factor 2 (FGF2) activity in FGF2-dependent capillary morphogenesis. We have injected control and transfected clones into nude nu/nu (CD-1) BR mice to study the differential tumor growth pattern. We observed a reduction of tumor growth in transfected clones, which was basically complete when clones expressing both molecules were simultaneously injected. The extent of tumor necrosis suggested an antiangiogenesis-dependent inhibition of tumor development.

Indexed as

AnimalsBlotting, WesternBreast NeoplasmsCell LineCell Line, TumorC-Reactive ProteinCulture Media, ConditionedEndothelial CellsFibroblast Growth Factor 2HumansMammary Neoplasms, ExperimentalMatrix Metalloproteinase 12MiceMice, Inbred C57BLMice, NudeNeovascularization, PathologicC-Reactive ProteinCulture Media, ConditionedFibroblast Growth Factor 2Matrix Metalloproteinase 12PentraxinsReceptors, Urokinase Plasminogen ActivatorSerum Amyloid P-Component

Identifiers

PMID19794969
PMCPMC2745676
OpenAlexW1244460611

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.